By blocking NNMT activity, the compound preserves nicotinamide availability for the NAD+ salvage pathway, leading to 1.2- to 1.6-fold increases in intracellular NAD+ concentrations
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In white adipose tissue of obese, insulin-resistant and aged mammals, NNMT is dramatically upregulated and because it consumes both the universal methyl donor (SAM) and the NAD precursor (nicotinamide), its hyperactivity simultaneously depletes the cellular methylation reserve and the NAD-salvage pool [1,2]